To verify the postoperative ultrastructural changes of the myotendinous nerve endings of feline extraocular muscles, which are known as proprioceptors. Sixteen recti of four cats were used and divided into three groups. In group A, eight lateral recti were recessed. In group B, four medial recti were resected by 10 mm from insertion to include the myotendinous junction. In group C, four medial recti were resected by 4 mm of muscle bellies only, without disturbing the myotendinous junction. Four weeks after surgery, specimens were examined with electron microscopy. In group A, overall neural structures were well maintained with slight axonal degeneration. In group B, only muscle fibers were observed without any regeneration of neural sprouts. In group C, axonal disintegration and shrinkage were evident. These results indicate that myotendinous nerve endings can be damaged in strabismus surgery, and that resection was more invasive than recession in disrupting myotendinous nerve endings.
Animals ; Cats ; Motor Neurons/ultrastructure ; Nerve Endings/*ultrastructure ; Neuromuscular Junction/*ultrastructure ; Oculomotor Muscles/*innervation/surgery ; Oculomotor Nerve/*ultrastructure ; *Ophthalmologic Surgical Procedures ; Receptors, Sensory/ultrastructure ; Strabismus/surgery ; Tendons/*innervation/ultrastructure

Axonal transport of mitochondria is critical for neuronal survival and function. Automatically quantifying and analyzing mitochondrial movement in a large quantity remain challenging. Here, we report an efficient method for imaging and quantifying axonal mitochondrial transport using microfluidic-chamber-cultured neurons together with a newly developed analysis package named "MitoQuant". This tool-kit consists of an automated program for tracking mitochondrial movement inside live neuronal axons and a transient-velocity analysis program for analyzing dynamic movement patterns of mitochondria. Using this method, we examined axonal mitochondrial movement both in cultured mammalian neurons and in motor neuron axons of Drosophila in vivo. In 3 different paradigms (temperature changes, drug treatment and genetic manipulation) that affect mitochondria, we have shown that this new method is highly efficient and sensitive for detecting changes in mitochondrial movement. The method significantly enhanced our ability to quantitatively analyze axonal mitochondrial movement and allowed us to detect dynamic changes in axonal mitochondrial transport that were not detected by traditional kymographic analyses.
Animals ; Axonal Transport ; physiology ; Cerebral Cortex ; cytology ; metabolism ; Drosophila melanogaster ; cytology ; metabolism ; Embryo, Mammalian ; Gene Expression ; Lab-On-A-Chip Devices ; Microscopy, Confocal ; Mitochondria ; metabolism ; ultrastructure ; Motor Neurons ; metabolism ; ultrastructure ; Movement ; Mutation ; Primary Cell Culture ; RNA-Binding Protein FUS ; genetics ; metabolism ; Rats ; Rats, Sprague-Dawley ; Software